Pathological erythrocyte deformability and aggregation reduces capillary perfusion and oxygen transfer to tissue, resulting in tissue ischemia or infraction. Shedding of procoagulant-rich microparticles from activated monocytes can accelerate the pathogenesis of atherothrombosis. Bone marrow-derived, circulating endothelial progenitor cells (EPC) is contributes to the maintenance of endothelial function and organ perfusion by mechanisms ranging from endothelial repair to angiogenesis. However, the different effects of AIT and moderate continuous training (MCT) on hemorheology, atherothrombosis or angiogenesis modulated by erythrocyte, monocyte or EPC in patients with CHF have been not investigated yet.